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Table 1 Examples of the role and the effect of deficiency of specific micronutrients on genomic stability [9–24]

From: Nutriomes and nutrient arrays - the key to personalised nutrition for DNA damage prevention and cancer growth control

Micronutrient/s Role in genomic stability Consequence of deficiency
Vitamin C, Vitamin E, antioxidant polyphenols (e.g. caffeic acid) Prevention of oxidation to DNA and lipid oxidation. Increased base-line level of DNA strand breaks, chromosome breaks and oxidative DNA lesions and lipid peroxide adducts on DNA.
Folate and Vitamins B2, B6 and B12 Maintenance methylation of DNA; synthesis of dTMP from dUMP and efficient recycling of folate. Uracil misincorporation in DNA, increased chromosome breaks and DNA hypomethylation.
Niacin Required as substrate for poly(ADP-ribose) polymerase (PARP) which is involved in cleavage and rejoining of DNA and telomere length maintenance. Increased level of unrepaired nicks in DNA, increased chromosome breaks and rearrangements, and sensitivity to mutagens.
Zinc Required as a co-factor for Cu/Zn superoxide dismutase, endonuclease IV, function of p53, Fapy glycosylase and in Zn finger proteins such as PARP. Increased DNA oxidation, DNA breaks and elevated chromosome damage rate.
Iron Required as component of ribonucleotide reductase and mitochondrial cytochromes. Reduced DNA repair capacity and increased propensity for oxidative damage to mitochondrial DNA.
Magnesium Required as co-factor for a variety of DNA polymerases, in nucleotide excision repair, base excision repair and mismatch repair. Essential for microtubule polymerization and chromosome segregation. Reduced fidelity of DNA replication. Reduced DNA repair capacity. Chromosome segregation errors.
Manganese Required as a component of mitochondrial Mn superoxide dismutase. Increase susceptibility to superoxide damage to mitochondrial DNA and reduced resistance to radiation-induced damage to nuclear DNA.
Calcium Required as cofactor for regulation of the mitotic process and chromosome segregation. Mitotic dysfunction and chromosome segregation errors.
Selenium Selenoproteins involved in methionine metabolism and antioxidant metabolism (e.g. selenomethionine, glutathione peroxidase I). Increase in DNA strand breaks, DNA oxidation and telomere shortening.
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